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Effect of hypoxia on the hypopnoeic and apnoeic threshold for CO2 in sleeping humans

机译:缺氧对睡眠人CO2的催眠和催眠阈值的影响

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摘要

class="enumerated" style="list-style-type:decimal">Rhythmic breathing during sleep requires that PCO2 be maintained above a sensitive hypocapnic apnoeic threshold. Hypoxia causes periodic breathing during sleep that can be prevented or eliminated with supplemental CO2. The purpose of this study was to determine the effect of hypoxia in changing the difference between the eupnoeic PCO2 and the PCO2 required to produce hypopnoea or apnoea (hypopnoea/apnoeic threshold) in sleeping humans.The effect of hypoxia on eupnoeic end-tidal partial pressure of CO2 (PET,CO2) and hypopnoea/apnoeic threshold PET,CO2 was examined in seven healthy, sleeping human subjects. A bilevel pressure support ventilator in a spontaneous mode was used to reduce PET,CO2 in small decrements by increasing the inspiratory pressure level by 2 cmH2O every 2 min until hypopnoea (failure to trigger the ventilator) or apnoea (no breathing effort) occurred. Multiple trials were performed during both normoxia and hypoxia (arterial O2 saturation, Sa,O2 = 80 %) in a random order. The hypopnoea/apnoeic threshold was determined by averaging PET,CO2 of the last three breaths prior to each hypopnoea or apnoea.Hypopnoeas and apnoeas were induced in all subjects during both normoxia and hypoxia. Hypoxia reduced the eupnoeic PET,CO2 compared to normoxia (42.4 ± 1.3 vs. 45.0 ± 1.1 mmHg, P < 0.001). However, no change was observed in either the hypopnoeic threshold PET,CO2 (42.1 ± 1.4 vs. 43.0 ± 1.2 mmHg, P > 0.05) or the apnoeic threshold PET,CO2 (41.3 ± 1.2 vs. 41.6 ± 1.0 mmHg, P > 0.05). Thus, the difference in PET,CO2 between the eupnoeic and threshold levels was much smaller during hypoxia than during normoxia (-0.2 ± 0.2 vs. -2.0 ± 0.3 mmHg, P < 0.01 for the hypopnoea threshold and -1.1 ± 0.2 vs. -3.4 ± 0.3 mmHg, P < 0.01 for the apnoeic threshold). We concluded that hypoxia causes a narrowing of the difference between the baseline PET,CO2 and the hypopnoea/apnoeic threshold PET,CO2, which could increase the likelihood of ventilatory instability.
机译:class =“ enumerated” style =“ list-style-type:decimal”> <!-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 睡眠期间进行有节奏的呼吸需要将PCO2维持在敏感的低碳酸血症性呼吸阈之上。缺氧会导致睡眠期间出现周期性呼吸,而补充二氧化碳可以防止或消除这种呼吸。这项研究的目的是确定缺氧对改变睡眠中人的气孔性PCO2和产生呼吸不足或呼吸暂停所需的PCO2(呼吸不足/呼吸暂停阈值)之间差异的影响。 缺氧的影响在七个健康,睡眠的人类受试者中检查了CO2的潮气末潮气分压(PET,CO2)和呼吸不足/呼吸暂停阈值PET,CO2。自发模式的双水平压力呼吸机通过每2分钟将吸气压力水平提高2 cmH2O直至呼吸不足(触发呼吸机失败)或呼吸暂停(无呼吸)而以小幅度减少PET,CO2的作用。在常氧和低氧期间(动脉血氧饱和度,Sa,O2 = 80%)以随机顺序进行了多次试验。呼吸不足/呼吸暂停阈值是通过平均每次呼吸不足或呼吸暂停前的最后三次呼吸的PET,CO2来确定的。 呼吸不足和呼吸暂停在正常人和缺氧期间均诱发。与正常氧相比,低氧降低了正常的PET,CO2(42.4±1.3 vs. 45.0±1.1 mmHg,P <0.001)。但是,无论是低呼吸阈值PET,CO2(42.1±1.4 vs.43.0±1.2 mmHg,P> 0.05)还是无呼吸阈值PET,CO2(41.3±1.2 vs.41.6±1.0 mmHg, P P ET,CO2的差异要比常氧时的小得多(-0.2±0.2 vs。 -2.0±0.3 mmHg,呼吸不足阈值的 P <0.01和呼吸机阈值的-1.1±0.2 vs。 -3.4±0.3 mmHg, P <0.01)。我们得出的结论是,低氧导致基线 P ET,CO2 与呼吸不足/呼吸暂停阈值 P ET之间的差异变窄,二氧化碳,这可能会增加通气不稳定的可能性。

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